The extent of tubular injury in untreated and vehicle-treated mice with glomerulonephritis was demonstrated by a 10-fold increase in the number of apoptotic (activated caspase-3+) tubular cells and a 300-fold increase in gene expression of kidney injury molecule-1 (KIM-1), which were both significantly reduced with BR-4628 treatment (Fig 3E and 3F). Here, HAVCR1 is linked to glomerulonephritis.